Normally, electrochemical activity within a human heart causes the organ's muscle fibers to contract and relax in a synchronized manner. This synchronized action of the heart's musculature results in the effective pumping of blood from the ventricles to the body's vital organs. In the case of ventricular fibrillation (VF), however, abnormal electrical activity within the heart causes the individual muscle fibers to contract in an unsynchronized and chaotic way. As a result of this loss of synchronization, the heart loses its ability to effectively pump blood. Defibrillators produce a large current pulse that disrupts the chaotic electrical activity of the heart associated with ventricular fibrillation and provides the heart's electrochemical system with the opportunity to re-synchronize itself. Once organized electrical activity is restored, synchronized muscle contractions usually follow, leading to the restoration of effective cardiac pumping.
First described in humans in 1956, transthoracic defibrillation has become the primary therapy for cardiac arrest, ventricular tachycardia (VT), and atrial fibrillation (AF). Monophasic waveforms dominated until 1996, when the first biphasic waveform became available for clinical use. Attempts have also been made to use multiple electrode systems to improve defibrillation efficacy. While biphasic waveforms and multiple-electrode systems have shown improved efficacy relative to monophasic defibrillation, there is still significant room for improvement: shock success rate for ventricular fibrillation (VF) remains less than 70% even with the most recent biphasic technology.
Cardiac fibrillation and defibrillation are still poorly understood and several hypotheses have been promulgated to explain the mechanisms of defibrillation. The concept termed the critical mass hypothesis posits that a defibrillation shock is successful because it extinguishes activation fronts within a critical mass of muscle by depolarizing all non-refractory tissue within a critical mass. The upper limit of vulnerability (ULV) theory hypothesizes that a shock will be successful when, in addition to terminating ventricular fibrillation (VF) wavefronts by prolonging refractoriness in the myocardium ahead of the wavefront, the shock also must not initiate new fibrillation-causing wavefronts at the border of the shock-depolarized region. A shock may be of sufficient intensity to depolarize the myocardium but not be of high enough intensity to prevent new activation fronts, thus resulting in a failed defibrillation attempt. The critical point hypothesis, related to the ULV theory, states that a shock must not create a critical point where a critical voltage gradient intersects with a critical point of refractoriness. These critical points are the initiation points of refibrillation. The “extension of refractoriness” theory states that the shock-induced depolarization of the fibrillating cardiac tissue extends the period of refractoriness to incoming VF wavefronts and as a result terminates VF. Other theories, related to the ULV hypothesis are “progressive depolarization” and “propagated graded (progressive) response cellular depolarization hypothesis”.
The theory of Virtual Electrode Polarization (VEP) describes the phenomena by which, because of current flow within a partially conductive medium (the myocardium) contained within another partially conductive medium (blood of the cardiac chambers, lungs, interstitial fluids and other organs within the thoracic cavity), myocardial polarization during defibrillation is characterized by the simultaneous presence of positive and negative areas of polarization adjacent to each other. “Phase Singularity” as defined within the context of VEP is a critical point that is surrounded by positively polarized (equivalent to “depolarized” in the conventional electrophysiology nomenclature), non-polarized and negatively polarized (equivalent to “hyperpolarized”) areas. These phase singularities are the source of re-initiation of fibrillation. Post shock excitations initiate in the non-polarized regions between the positively and negatively polarized areas through a process termed “break excitation.” The break excitations propagate through the shock-induced non-polarized regions termed “excitable gaps”, and if the positively polarized regions have recovered excitability, then a re-entrant circuit at which fibrillation may initiate is formed. The upper limit of vulnerability (ULV) is attained when the areal extent of the excitable gaps is sufficiently minimized, or the shock induced voltage gradient is sufficient to cause rapid propagation of the excitation in the excitable gap, or the extension of refractoriness is sufficient to prevent further advance of the break excitations into the depolarized tissue. With biphasic defibrillation, the second phase of the shock tends to nullify the VEP effect by depolarizing the negatively polarized tissue. Since less energy is needed to depolarize repolarized tissue than further depolarize already depolarized tissue, effective biphasic defibrillation achieves nearly complete depolarization of the myocardium by reversing the negative polarization while maintaining the positive polarization. There remain, however, excitable gaps with biphasic waveforms, albeit reduced in scope relative to monophasic waveforms.
Theoretical approaches to stimulation employing current summation of multiple current sources have been used in the past to produce in the overlap region an additive current or integrated myocardial response sufficient to cause stimulation or defibrillation while the singular current vectors would not. The approach does not address the issue that insufficiently stimulated tissue may remain in the excitable gap that may result in refibrillation.
The concept of current equalization has been promulgated as a means of understanding stimulation. The general approach is to equalize the current distribution across the heart and concentrate the current in the muscular areas of the heart. This approach does not address the generation of the excitable gap, which will still be present. As understood within the context of the VEP effect, uniform current distributions still result in an excitable gap. In fact, a uniform current distribution is not an especially relevant concept within the context of a physiological system such as that of the human thorax where conductances of the organs, muscle, fluids and bone may vary by a factor of 100. Within such a system, current distributions will not be uniform. Even in a simplified, two-conductance system, an applied uniform field will result in a non-uniform current distribution due to the difference in conductances.
The technique of superposed, multiple vector physiologic tissue stimulation has been employed as early as 1948 by Nemec, as disclosed in U.S. Pat. No. 2,622,601, in which a nerve or muscle stimulator is described employing two stimulation waveform generators with multiple sets of electrode. Each waveform is an alternating current electrical signal with the difference between the two frequencies set to 1-100 Hz. In the areas of tissue that are exposed to currents from both sources—the regions of current superposition—a beat frequency equal to the frequency difference will be generated that is capable of stimulating the physiological tissue. U.S. Pat. No. 3,774,620 added the concept of superposition of two or more AC currents that by themselves have no stimulative effect, the currents differing from each other by a low value, with an optimum interference in the treatment area. Similar methods were employed in U.S. Pat. Nos. 3,774,620, 3,895,639, 4,023,574, and 4,440,121. In these and much of the subsequent art, the regions of interest were those areas where the current from the multiple sources overlapped. The summation current in the overlap region would result in a beat frequency or additive current, which would be sufficient to cause stimulation while the singular current vectors would not.
The earliest cardioverters and defibrillators generated either a single burst of alternating current or a single pulse for application to the heart to cause cardioversion or defibrillation. However, the use of multiple pulses to accomplish cardioversion or defibrillation has also been extensively researched. U.S. Pat. No. 3,605,754 discloses an early double pulse heart defibrillator employing two capacitors that are successively discharged between a single pair of electrodes. Multiple-electrode systems have been employed for implantable pacemakers and defibrillators. For example, sequential pulse multiple electrode systems are disclosed in U.S. Pat. Nos. 4,291,699, 4,641,656, 4,708,145, 4,727,877 4,932,407, and 5,107,834. Sequential-pulse systems operate based on the assumption that sequential defibrillation pulses, delivered between differing electrode pairs have an integrative effect, due to the non-linear action potential response of cardiac tissue, such that the overall energy requirements to achieve defibrillation are less than the energy levels required to accomplish defibrillation using a single pair of electrodes. An alternative approach to multiple-electrode, sequential-pulse defibrillation is disclosed in U.S. Pat. No. 4,641,656. One electrode pair may include a right ventricular electrode and a coronary sinus electrode, and the second electrode pair may include a right ventricular electrode and a subcutaneous patch electrode, with the right ventricular electrode serving as a common electrode to both electrode pairs. An alternative multiple-electrode, simultaneous-pulse system is disclosed in U.S. Pat. No. 4,953,551, employing right ventricular, superior vena cava and subcutaneous patch electrodes. U.S. Pat. No. 4,953,551 discloses simultaneous delivery of pulses between the superior vena cava and the right ventricle and between the right ventricle and a subcutaneous electrode. In U.S. Pat. No. 5,163,427, two capacitor banks are provided which are simultaneously charged and then successfully or simultaneously discharged between different pairs of electrodes.
French Patent No. 2,257,312 discloses sequential pulse defibrillators employing multiple electrodes arranged in and around the heart. In that disclosure, alternating current (AC) defibrillation pulses are sequentially delivered such that each successively activated electrode pair defines a pulse vector, and such that the pulse vectors scan in a rotational fashion through the heart tissue. Pulses are delivered immediately following one another, or may overlap one another for some unspecified period. U.S. Pat. No. 5,324,309 describes overlapping dual pathway pulses where there is an intermediate current vector during the overlap period. U.S. Pat. No. 5,766,226 describes a similar configuration in which the intermediate current vector changes direction and is made to cycle back and forth during the shock pulse. A similar configuration is described in U.S. Pat. No. 5,800,465. U.S. Pat. No. 5,330,506 describes a multi-pathway pacing method where each individual path is a subthreshold stimulus while the current level in the region of superposition is suprathreshold. The current vector in the region of superposition can be steered by varying the timing of the individual pulse onsets. U.S. Pat. No. 5,431,688 describes a multi-electrode, focused waveform, with interposed pulse trains. These techniques have similar deficits in that, while they are able to reduce the excitable gap to some extent via the rotating vector produced by the overlapping of the currents, regions of excitable gap will remain that can still trigger refibrillation.
U.S. Pat. No. 6,148,233 describes a multi-contact electrode composed of multiple small active areas, each active area of a size too small to defibrillate. Each active area is connected to the same current source. Division of the electrode into plural active areas is intended to provide a means of reducing skin sensitization from long-term wear of the electrodes.